title: Left ventricular hypertrophy and endothelial dysfunction in chronic kidney disease.
abstract: Aim Mortality, predominantly due to cardiovascular events, is high in patients with chronic kidney disease (CKD) and left ventricular hypertrophy (LVH) is a strong risk factor. Vascular endothelial dysfunction (ED) is common in CKD, but its potential contribution to LVH in non-dialysis CKD is unknown. This study investigated the association of ED with LVH in non-dialysis CKD patients.
  
  
  RESULTS
  We studied 30 CKD patients (17 pre-dialysis and 13 renal transplant recipients) and 29 age-gender-matched controls. In both groups, high-sensitivity C-reactive protein (hsCRP) levels, systemic ED (brachial artery flow-mediated dilatation, FMD), and LVH using two-dimensional echocardiography were measured. LV mass index (LVMI) was calculated using Penn formula and indexed by height. CKD patients had higher CRP levels (3.9 ± 2.8 vs. 1.0 ± 0.7 mg/L; P < 0.001), reduced FMD (3.2 ± 2.1 vs. 6.1 ± 1.9%; P < 0.001), and increased LVMI (146.1 ± 40.2 vs. 105.3 ± 26.2 g/m; P < 0.001), compared with controls. In CKD patients, LVMI increased with decreasing FMD (r = -0.371; P = 0.043) and FMD decreased with increasing CRP (r = -0.741; P < 0.001). Patients with low FMD <2.3% had higher CRP and LVMI (161.9 ± 48.9 vs. 130.4 ± 20.7 g/m; P = 0.033), compared with CKD patients with FMD ≥2.3%. There was no significant difference in age, blood pressure, cholesterol, FMD, and LVMI between pre-dialysis and post-renal transplant CKD patients. In multivariate regression, the relationship between LVMI and FMD remained significant after adjusting for age, diabetes, and smoking (adjacent beta = -0.396; P = 0.004).
  
  
  CONCLUSIONS
  This pilot study demonstrates for the first time a relationship of ED with LVH in non-dialysis CKD patients; suggesting but not proving a cause-effect relationship.
authors.affiliation: Renal and Transplantation Unit, St George's Healthcare NHS Trust, Blackshaw Road, Tooting, London SW19 8TN, UK.
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Poulikakos
authors.forename: Louise
authors.initials: L
authors.lastname: Ross
authors.forename: Alejandro
authors.initials: A
authors.lastname: Recio-Mayoral
authors.forename: Della
authors.initials: D
authors.lastname: Cole
authors.forename: Jocelyn
authors.initials: J
authors.lastname: Andoh
authors.forename: Nihil
authors.initials: N
authors.lastname: Chitalia
authors.forename: Rajan
authors.initials: R
authors.lastname: Sharma
authors.forename: Juan
authors.initials: J
authors.lastname: Carlos Kaski
authors.forename: Debasish
authors.initials: D
authors.lastname: Banerjee
mesh_terms: D001916:Brachial Artery / Q000000981:diagnostic imaging; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D004452:Echocardiography / Q000379:methods*; D004730:Endothelium, Vascular / Q000473:pathology; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000000981:diagnostic imaging* / Q000209:etiology*; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications* / Q000628:therapy; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D002097:C-Reactive Protein
keywords: chronic kidney disease; endothelial function; left ventricular hypertrophy